ZR-75-1 estrogen independent breast cancer cell line panel (2)
Invented at Erasmus Medical Center
- Datasheet
- References (7)
- Inventor Info
Info
| Catalogue Number | 154645 |
| Antigen/Gene or Protein Targets | BCAR1, BCAR3, AKT1, AKT2, BCAR4, GRB7, EGFR, HRAS, PDGFRA, PDGFRB, RAF1 |
| Parental Line | ZR-75-1 |
| Host | Human |
| Tissue | Breast |
| Disease Keywords | Mammary ductal carcinoma, estrogen independent |
| Model | Cancer Model |
| Relevance |
Endocrine therapy of breast cancer has been applied widely and proven to be effective. However, in many instances endocrine treatments ultimately fail due to the development of an estrogen-independent therapy resistant phenotype. To elucidate the molecular mechanism underlying this endocrine therapy failure, the laboratory of Lambert Dorssers applied different genetic screens to identify the main genes conferring estrogen independence. Out of 15 candidate BCAR genes, several including BCAR1, BCAR3, AKT1, AKT2, BCAR4, GRB7, EGFR, HRAS, PDGFRA, PDGFRB and RAF1 were shown to directly underlie estrogen independence by transfection into the ZR-75-1 breast cancer cell line resulting in a panel of 16 cell lines (Cat No 154621-154635, 154642) These cell lines are a powerful tool for studying the molecular and cellular mechanisms of breast tumour progression, therapy resistance and to test the effectiveness of novel drugs to combat different modes of anti-estrogen insensitivity. |
| Production Details | Full length cDNA of the relevant gene was introduced in the estrogen-dependent ZR-75-1 cell line by transfection with lipofectamine |
| Conditional | No |
| Research Area | Cancer, Drug Discovery & Development |
| Recommended Growing Conditions | RPMI 1640 medium supplemented with 10% heat-inactivated bovine serum (RBCS) and 1 nM 17β-estradiol |
| Notes |
These cell lines are resistant to Geneticin, which may be included in the culture medium to ensure that the expression vector is retained by the cells. As a consequence of the presence of a BCAR genes, these cells can also proliferate in the absence of estrogen or even in the presence of anti-estrogens. |
References: 7 entries
Godinho et al. 2011. J Cell Physiol. 226(7):1741-9. PMID: 21506106.
van Agthoven et al. 2010. Endocr Relat Cancer. 17(1):215-30. PMID: 19966015.
van Agthoven et al. 2009. Breast Cancer Res Treat. 114(1):23-30. PMID: 18351453.
Meijer et al. 2006. Mol Cancer Res. 4(6):379-86. PMID: 16778085.
Brinkman et al. 2000. J Natl Cancer Inst. 92(2):112-20. PMID: 10639512.
van Agthoven et al. 1998. EMBO J. 17(10):2799-808. PMID: 9582273.
van Agthoven et al. 1992. Cancer Res. 52(18):5082-8. PMID: 1516065.
Add a reference
References: 7 entries
Godinho et al. 2011. J Cell Physiol. 226(7):1741-9. PMID: 21506106.
van Agthoven et al. 2010. Endocr Relat Cancer. 17(1):215-30. PMID: 19966015.
van Agthoven et al. 2009. Breast Cancer Res Treat. 114(1):23-30. PMID: 18351453.
Meijer et al. 2006. Mol Cancer Res. 4(6):379-86. PMID: 16778085.
Brinkman et al. 2000. J Natl Cancer Inst. 92(2):112-20. PMID: 10639512.
van Agthoven et al. 1998. EMBO J. 17(10):2799-808. PMID: 9582273.
van Agthoven et al. 1992. Cancer Res. 52(18):5082-8. PMID: 1516065.
Add a reference
